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Hypophosphatasia (HPP) is the heritable dento-osseous disease caused by loss-of-function mutation(s) of the gene ALPL that encodes the tissue-nonspecific isoenzyme of alkaline phosphatase (TNSALP). TNSALP is a cell-surface homodimeric phosphomonoester phosphohydrolase expressed in healthy people especially in the skeleton, liver, kidneys, and developing teeth. In HPP, diminished TNSALP activity leads to extracellular accumulation of its natural substrates including inorganic pyrophosphate (PPi), an inhibitor of mineralization, and pyridoxal 5'-phosphate (PLP), the principal circulating form of vitamin B (B).

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The aim of the review was to describe a complex microstructure and biomechanical properties of the articular cartilage as well as a current review of its pathologies encountered in veterinary practice. The articular cartilage with its unique features: complex microarchitecture, significant mechanical durability and elasticity, lacking blood, lymphatic vessels, and innervation, seems to stand in contradiction to the laws of biology. It can be involved in a vast majority of diseases, from osteoarthrosis as a result of natural aging process to more complex in nature like osteochondromatosis.

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Regenerating epidermis and spinal cord is essential to maintain tail regeneration in lizards. The effects of vitamin A, an inhibitor of epithelial cornification, have been studied in lizards during tail regeneration. The injection of high doses of vitamin A induces regeneration of a thinner tail with gummy consistency and suppression of the formation of a normal cartilaginous axial skeleton.

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Background: A vitamin A derivative, 13-cis-retinoic acid (isotretinoin), has been administered to treat several types of pediatric cancer and has improved survival rates in patients despite being known to induce premature epiphyseal closure. As the number of patients treated by 13-cis-retinoic acid increases, demands for salvage treatment after systemic retinoid therapy are emerging. However, few studies have described the surgical treatment of this disease.

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Vitamin A decreases the anabolic bone response to mechanical loading by suppressing bone formation.

FASEB J

April 2019

Department of Internal Medicine and Clinical Nutrition, Centre for Bone and Arthritis Research, Institute for Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.

Increased vitamin A consumption is associated with decreased cortical bone mass and increased fracture risk in humans. Rodent studies have demonstrated that hypervitaminosis A increases cortical bone resorption, whereas the importance of the effects on bone formation is less well defined. We used an experimental model of increased bone formation by loading of the tibiae to investigate the effect of vitamin A on bone formation.

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